Stroke is a manifestation of injury to the brain which is commonly secondary to atherosclerosis or hypertension, and is the third leading cause of death in the United States. Stroke can be categorized into two types, ischemic stroke and hemorrhagic stroke. Additionally, a patient may experience transient ischemic attacks, which are in turn a high risk factor for the future development of a more severe episode.
Examples of ischemic stroke encompass thrombotic, embolic, lacunar and hypo-perfusion types of strokes. Thrombi are occlusions of the arteries created in situ within the brain, while emboli are occlusions caused by material from a distant source, such as the heart and major vessels, often dislodged due to myocardial infarct or atrial fibrillation or carotid disease or surgical or percutaneous intervention. Thrombi or emboli can result from atherosclerosis or other disorders, for example arteritis, and lead to physical obstruction of arterial blood supply to the brain. Lacunar stroke refers to an infarct within non-cortical regions of the brain. Hypo-perfusion embodies diffuse injury caused by non-localized cerebral ischemia secondary to low cerebral perfusion, typically caused by myocardial infarction, arrhythmia, blood loss or prolonged low blood pressure.
Hemorrhagic stroke is caused by intra cerebral or subarachnoid hemorrhage, i.e., bleeding in to brain tissue, following blood vessel rupture within the brain or venous thrombosis. Intra cerebral and subarachnoid hemorrhages are subsets of a broader category of hemorrhage referred to as intracranial hemorrhage.
Intra cerebral hemorrhage is typically due to chronic hypertension and a resulting rupture of an arteriosclerotic vessel. Stroke-associated symptom(s) of intra cerebral hemorrhage are abrupt, with the onset of headache and steadily increasing neurological deficits. Nausea, vomiting, delirium, paralysis, seizures and loss of consciousness are additional common stroke-associated symptoms.
In contrast, most subarachnoid hemorrhage is caused by head trauma or aneurysm rupture which is accompanied by high-pressure blood release which also causes direct cellular trauma. Prior to rupture, aneurysms may be asymptomatic, or occasionally associated with headaches. However, headache typically becomes acute and severe upon rupture and may be accompanied by varying degrees of neurological deficit, vomiting, dizziness, and altered pulse and respiratory rates, photophobia and severe headache and or neck stiffness.
Current diagnostic methods for stroke include costly and time-consuming procedures such as non-contrast computed tomography (CT) scans, electrocardiogram, magnetic resonance imaging (MRI) and angiography. Determining the immediate cause of stroke is difficult. CT scans can detect parenchymal bleeding greater than 5 mm and 95% of all subarachnoid hemorrhages. CT scans often cannot detect ischemic strokes until 6 hours from onset, depending on infarct size. CT only identifies 48% of acute strokes in the first 48 hours. MRI may be more effective than CT scan in early detection of ischemic from hemorrhagic stroke, and is not widely available. Angiography is a definitive test to identify stenosis or occlusion of large and small cranial blood vessels, and can locate the cause of subarachnoid hemorrhages, define aneurysms, and detect cerebral vasospasm. It is, however, an invasive procedure and is also limited by cost and availability.
Immediate diagnosis and care of patients experiencing stroke can be critical. For example, tissue plasminogen activator (tPA) given within three hours of symptom onset in ischemic stroke is beneficial for selected acute stroke patients. In contrast, thrombolytics and anticoagulants are strongly contraindicated in hemorrhagic strokes. Thus early differentiation of ischemic events from hemorrhagic events is imperative. Moreover, delays in confirmation of stoke diagnosis and identification of stroke type limit the number of patients that may benefit from early intervention therapy. In addition, continuous monitoring of stroke patients is not possible with CT or MRI scanners, thus only one snapshot in time is available for diagnosis and treatment. Clinical observations are the basic tool that is used to monitor the progress of stroke patients.
Early detection of an aneurysm is beneficial as it can frequently be treated either by a surgical procedure of clip occlusion or by endovascular coil embolism. Presently, approximately three quarters of patients are treated with clip occlusion, the remainder with endovascular coil embolism. Either surgery, particularly the endovascular procedure, can by performed with low complication rate and high rate of success.
Once an aneurysm ruptures, however, the patient declines rapidly due to major brain injury, and over 50% of aneurysm rupture patients die acutely. Thus detection of at risk aneurysms is of great benefit. A physician faced with possible aneurysm warning signs must judge whether the symptoms warrant the trauma, expense and morbidity of contrast angiography.
Ferguson, in J. Neurosurg. 36:560-563 (1972), suggested detecting aneurismal signals by recording sounds from aneurysms exposed at operations using a cardiac phono-catheter. Kosugi et al., in Stroke 14 (1) 37-42 (1983), disclosed the use of a “cement wall microphone”, (contact accelerometer) in contact with the cranium and the teeth in an attempt to detect aneurysms.
However, devices and methods to date have not localized the detected vascular conditions and do not present the collected data in a clinically useful way.
Thus, despite these known devices, there remains a need for an acoustic detector that is designed to more effectively record, analyze, localize and present, in a clinically useful manner, cerebral arterial and venous conditions.